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Pharmacology > B3 > Flashcards

B3 Flashcards

1
Q

List typical and atypical neuroleptics

A

Typical neuroleptics : a) High potency drug - Haloperidol , Fluphenazine
b)Low potency drug - Chlorpromazine

Atypical antipsychotics - a) Clozapine , Risperidone , Olanzapine , Quetiapine

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2
Q

Explain the mechanism of action of chlorpromazine

A

A)Mesolimbic pathway - Block dopamine , Alleviate positive symptoms

B)Mesocortical pathway - Block dopamine D2 receptor , Worsen negative symptoms

C)Chemoreceptor trigger zone pathway - Block dopamine D2 receptors , prevent vomiting

D)Tuberoinfundibular pathway - Hyperprolactinemia (Gynaecomastia ), Inhibit release of FSH & LH

E)Medullary periventricular pathway -Metabolic effect : Changes in eating behaviour and weight gain

F)Nigrostriatal pathway -Extrapyramidal symptoms

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3
Q

List therapeutic uses of antipsychotics

A

Psychiatric uses :
A) Schizophrenia
B) Acute mania and bipolar disorder (BPD)
C)Psychotic depression

Non Psychiatric uses
A) Pruritis - acts by blocking H1 receptors
B) Intractable hiccups ( hiccough)

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4
Q

Advantages of atypical antipsychotics over typical antipsychotics

A

A) Minimal risk of extrapyramidal side effects
B) Minimal risk of developing of Hyperprolactinemia
C)Less autonomic side effect
D) Effective against “negative” symptoms due to serotonin receptors blockade

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5
Q

Specific side effect of atypical psychotics

A

Agranulocytosis , Sedation , Weight gain , Paradoxical hypersalivation , Risk diabetes , Hyperprolactinemia

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6
Q

List drugs used in the treatment of bronchial asthma based on their MOA.

A

***1) Bronchodilators
A)Short-acting bronchodilators
- short acting beta 2- agonists ( SABA ) : Salbutamol, Terbutaline
- Phosphodiesterase (PDE III) inhibitors : Aminophylline , Theophylline
- Muscarinic receptor antagonists : Ipratropium

B) Long acting bronchodilators

  • Long acting beta 2 agonists (LABA): Salmeterol , Formoterol.
  • Phosphodiesterase (PDE II) inhibitors : Theophylline SR
  • Muscarinic receptor antagonists : Tiotropium

***2)Anti-inflammatory agents : Glucocorticoid
A) Systemic : Hydrocortisone & Prednisolone
B) Inhalation : Budesonide , Fluticasone , Beclomethasone.
C) Oral : Prednisolone , metyl Prednisolone, Dexamethasone , Betamethasone

3) Mast cell stabilizers
- Ketotifen

4) Monoclonal IgE antibody
- Omalizumab

5) Leukotriene (LT) receptor antagonists
- Montelukast , Zafirlukast

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7
Q

Explain the anti asthmatic action of following drugs : beta 2 agonists,Muscarinic receptor antagonist, Phosphodiesterase III inhibitors & glucocorticoids.

A

A)Beta 2 agonists :

  • bind to beta2 receptors on bronchial smooth muscle -> stimulate adenylyl cyclase -> bronchial smooth muscle relaxation
  • inhibit the release of inflammatory mediator from mast cells by acting on beta 2 receptors
  • Inhibit microvascular leakage
  • Increase mucociliary clearance

B) Muscarinic receptor antagonists
- inhibits the effects of acetylcholine in larger airways by blocking M3 receptor -> bronchodilation & decrease the secretion of mucus

C) Phosphodiesterase III inhibitors

  • PDE inhibitors competitively inhibit the PDE enzyme -> decrease cAMp degradation -> increase cAMP -> bronchial smooth muscle relaxation.
  • Block adenosine receptors on bronchial smooth muscle -> increase the formation of cAMP -> contribute to brondilation

D) Glucocorticoids

  • induce lipoprotein -> inhibit phospholipids A2 -> prevent the formation of various inflammatory mediators
  • also suppress the inflammatory response
  • Can up regulate beta 2 receptor
  • Reduce mucosal edema
  • reduce bronchial hyper responsiveness
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8
Q

List the adverse effects of beta 2 agonists

A

A) Tremors due to stimulation of beta 2 receptors in skeletal muscle -> enhanced firing of muscle spindles
B) Tachycardia and palpitation due to the stimulation of beta 1 receptors in the heart
C) Hyperglycemia occur due to increase release of glucagon in diabetes patient
D) Hyperkalaemia - stimulation of beta 2 receptor cause shifting of K+ into cells especially into skeletal muscle

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9
Q

Explain the adverse effects of inhalational glucocorticoids

A
  • Dryness of mouth
  • Dysphonia due to local effects of glucocorticoids on vocal cord
  • Oropharyngeal candidiasis due to immunosuppression of cells those exposed to inhaled glucocorticoid and lack of oral hygiene
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10
Q

List the drugs terminate the attack of angina

A

Sublingual GTN , Sublingual Isosorbide dinitrate

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11
Q

List the therapeutic uses of nitrates with their route of administration

A

A) Angina pectoris : sublingual GTN 500 mcg ,
B) Heart failure : more commonly used reason than angina
-reduce the preload and hence reduce the pulmonary congestion and improves CO
C) Myocardial infarction
D) Cyanide poisoning

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12
Q

State the adverse effect of nitrates

A

A) throbbing headache
B) nitrate tolerance : develops when used continuously as infusion or patch
- tolerance due to exhaustion of SH groups which release NO from nitrates
- Give 8 hrs of nitrate free intervals to prevent tolerance
- Drug interaction with sildenafil ( PDE V inhibitor) : potential of hypotension action of nitrates leading to MI and sudden death

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13
Q

State the example drugs of calcium channels blocker

A

A) Dihydropyridines : more selective on vascular smooth muscle ( nifedipine , amlodipine)
B)Non- dihydropyridines : more selective on cardiac muscle ( verapamil , diltiazem)

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14
Q

Explain the pharmalogical action of Calcium channel blockers

A

CCb block the voltage gated L type calcium channels , reduces calcium availability and hence inhibits vascular smooth muscle contraction or conduction in SA node and AV nodes

  • reduce heart rate , contractility, conductivity and hence the workload on the heart which lead to (*reduce O2 demand) during angina.
  • CCB relax vascular smooth muscle and cause coronary artery dilation leading to (*increased O2 supply) in angina.
  • dilating the peripheral arteries , they decrease afterload on heart and hence the myocardial oxygen demand in angina.
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15
Q

Non-dihydropyridine and (……) combination is contraindicated

A

( beta blocker )

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16
Q

Explain the beta blocker in angina

A

A) Reduce workload and hence myocardialO2 demand causing relief from angina pain.
B) Decreased heart rate also increase diastolic coronary perfusion , this increase myocardial O2 supply - relief from angina

*** Non selective beta blocker are contraindicated in variant angina : inhibition of beta 2 mediated coronary vasodilation and unopposed alpha action causing vasospasm

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17
Q

List the antidepressant based on their mechanism of action

A

A) Selective Serotonin Reuptake Inhibitors (SSRI)
-Fluoxetine & Fluvoxamine
B) Serotonin and noradrenaline reuptake inhibitor (SNRI)
-Duloxetine & Venlafaxine
C) Tricyclic antidepressants
- Amitriptyline , Nortriptyline

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18
Q

Explain about the mechanism of TCAs.

A

Tricyclic antidepressants ( TCAs) inhibit norepinephrine transporter ( NeT) and serotonin transporter (SERT) , then it block the reuptake of NE and 5-HT into their respective neurons —> more availability and a longer stay of NE and 5-HT at their respective receptor site —-> antidepression action

  • Clinical benefit appear after several weeks of treatment , implicating neuroadaptive changes in receptor regulation and second messenger system
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19
Q

List the adverse effects of TCAs

A

A) inhibit the histamine H1 receptor —> sedation

B) inhibit the Muscarinic receptors —-> atropine-like side effects ( dry mouth , tachycardia , urinanry retention , hallucination

C) inhibit the alpha 1 receptors —> orthostatic hypotension

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20
Q

List the therapeutic uses of TCAs

A

-not first line therapy

Indication :

  • phobic disorder
  • chronic neuropathic pain
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21
Q

Explain the mechanism of action of Selective Serotonin reuptake inhibitor (SSRI)

A
  • blocks the reuptake of 5-HT into serotoninergic neurons —-> more availability and a longer stay of 5-HT at 5-HT receptors in the CNS and enhance serotonergic activity —> antidepressant action

***First line drugs in the treatment of depression

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22
Q

List the adverse effects of SSRIs

A

A) GI symptoms like nausea , vomiting and diarrhoea
***B) Sexual dysfunction : impotence , loss of libido
C) Suicidal ideation
D) Insomnia

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23
Q

State the advantages of SSRI over TCAs

A
  • inhibit serotonergic transporter (SERT) only
  • don’t have antocholinergic action ( X dry mouth , X urinary retention , X constipation )
  • Have no alpha blocking actions ( no postural hypotension)
  • have no H1 blocking action ( no sedation )
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24
Q

State therapeutic uses of antidepressants

A 
D - Depression 
E - Enuresis (Imipramine) 
P -Phobia
R -Recurrent panic attacks 
E- eating disorder
S - smoking cessation  
S- stress disorder
I - impulse disorder 
O - Obsessive compulsive disorder 
N - neuropathic pain
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25
Q

Where histamine mainly store?

A

Mast cell , basophil , eosinophil and enterochromaffin like cell (ECL cells)

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26
Q

List the first generation and second generation of antihistamines

A

First generation - Diphenhydramine , Promethazine , Doxylamine

Second generation - Fexofenadine , Cetirizine , Levocetirizine

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27
Q

List the therapeutic use of 1st generation antihistamine

A

A) Allergic reactions -block the effects of released histamine by blocking H1 receptors
-used to treat or prevent the symptoms of allergic rhinitis and urticaria

B)Motion sickness - 1st generation antihistamine( diphenhydramine , promethazine) are used because their additional anti Muscarinic ( M1 receptor blocking) property.

C) Vomiting - (hydroxyzine & promethazine) used because of their anti Muscarinic property
-prevent the transmission of impulses from GIT to vomiting centre. Doxylamine is used for morning sickness as it has no teratogenic property.

D) Cough -provide symptomatic relief by sedative and anticholinergic property.

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28
Q

State the advantages of second generation antihistamine over the 1st generation of antihistamine

A

A)Longer duration of action
B) Less sedating
C) Poor permeability to BBB - devoid of CNS depressant property
D) Devoid of anticholinergic side effects

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29
Q

List the antiepileptics drugs treat various types of seizures

A

Phenytoin , carbamazepine , sodium valproate , gabapentin & pregabalin

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30
Q

Explain the mechanism of action of phenytoin

A

A) Phenytoin binds to the voltage dependent Na channels in inactivated state.
B) Prolongs the inactivated state of Na channels
C) Decrease the Na levels and decrease the neuronal excitability.
D) Prevent the spread of high frequency firing

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31
Q

Explain the pharmacokinetics of phenytoin

A
  • route of administration Oral and IV
  • absorption slowly from intestine
  • Widely distributed in the body
  • highly bound to plasma albumin
  • completely metabolised in liver by hydroxylation & glucuronide conjugation.
  • microsomal enzyme induction cause many drug interaction
  • Zero order kinetics and cause accumulation leading to toxicity.
  • Therapeutic drugs monitoring of phenytoin therapy is essential.
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32
Q

List the Acute toxicities and chronic toxicities of phenytoin

A

Acute toxicity

  • Early signs : Nystagmus , blurred vision
  • Diplopia & Ataxia

Chronic toxicity

  • Gum hyperplasia : due to inhibition of collagenase enzyme by phenytoin
  • Coarsening of facial features
  • Hirsutism: increase of androgens
  • Hyperglycemia : due to insulin release
  • Ricket and osteomalacia : increase metabolism of calciferol and leads to Vit D deficiency.
  • Megaloblastic anaemia due to decrease folate deficiency.
  • Vit K deficiency
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33
Q

List the mechanism action of carbamazepine

A

A) Binds to voltage dependent Na channels to their inactivated state .

B) prolongs their inactivated state of Na channels

C) Decrease Na levels at neurons and decrease neuron excitability

D) Prevent the spread of high frequency firing

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34
Q

List the adverse effect of carbamazepine

A
  • Hypersensitivity reactions
  • Water retention and hyponatremia
  • Teratogenicity : delayed development of foetus
  • Rash and hyponatremia
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35
Q

List the Therapeutic Use of Carbamazepine

A
  • Complex partial seizure
  • Generalised tonic clonic seizure
  • Simple partial seizure
  • **-Trigeminal neuralgia
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36
Q

Explain the mechanism of action of sodium valproate

A

A) Phenytoin like action : block the sodium channel
B) Block T type calcium channel in thalamus
C) Increase activity of GABA in the brain by :
I) Increased synthesis of GABA by stimulating GAD ( Glutamic Acid Decarboxylase)
II) Prevent mechanism of GABA by inhibiting enzyme GABA transaminase & succinic semialdehyde dehydrogenase ( Protects GABA from presynaptic degradation )

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37
Q

State the adverse effects of sodium valproate

A
  • ** Teratogenic effects neural tube defects —> incidence of spina bifida , orofacial and digital abnormalities.
  • definite teratogen and should be avoided not only in pregnancy but also in childbearing age group
Mnemonics 
V-vomiting
A- Alopecia
L-liver damage 
P-Pancreatitis
R-Rash
O-Obesity
A-Agranulocytosis 
T- Tremors
E- Epigastric pain
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38
Q

List diuretics based on their mechanism of actions n

A

A) Proximal convoluted tubules (Site 1)
-Carbonic anhydride inhibitors: Acetazolamide

B) All segments of nephron , except thick ascending loop of Henle.
-Osmotic diuretic : Mannitol , glycerol

C) Thick ascending limb of loop of Henle
-Loop diuretics / High ceiling diuretics : Furosemide/ Frusemide , bumetanide , torsemide , ethacrynic acid

D) Early part of the distal tubule
- Thiazide : Hydrochlorothiazides, Chlorothiazide , benzthiazide

E) Late distal tubules and collecting duct
- potassium sparing diuretics

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39
Q

Explain the mechanism of action of acetazolamide (carbonic anhydrase inhibitors)

A

A) Predominant place is the epithelial cell of proximal convoluted tubules where it catalyse the dehydration of H2CO3.

B) By blocking carbonic anhydrase , inhibitor blunt NaHCO3 re absorption and cause diuresis.

C)Carbonic anhydrase inhibitor ( acetazolamine ) inhibit the carbonic anhydrase enzyme in proximal tubules —> prevent the formation of H+ —> Na- H+ exchange is prevented —>. Na+ is excreted out with the bicarbonate & water

40
Q

State the therapeutic uses of carbonic anhydrase inhibitor ( acetazolamide )

A

A) Acute glaucoma ( reduction of intraocular pressure )
-inhibition of carbonic anhydrase reduces the formation of aqueous humour and lower intraocular pressure.

B) High altitude sickness

  • at high altitude , the normal hyperventilatory response to falling oxygen tension is inhibited & alkalosis is induced.
  • Acetazolamide works by acidifying the blood & reducing respiratory alkalosis associated with high elevation, thus increasing respiration & arterial oxygenation & speeding acclimatisation.

C) Urinary alkalinization
- used as second line drugs for tonic-clonic and partial epileptics

41
Q

Explain the mechanism of action of mannitol (osmotic diuretics )

A

A) Draw water from tissues by osmotic actions which results in increased excretion of water and electrolytes

B) I) increase the osmolarity of plasma
II) shift the intracellular fluid by osmotic effect from intracellular component ( from brain and eyes ) to ECF
III) reduce the intracranial pressure & intraocular pressure in patients with cerebral oedema & acute congestive glaucoma.

42
Q

List the therapeutic uses of mannitol ( osmotic diuretics )

A
  • treat oliguria state in shock or crush injury and to prevent onset of renal failure
  • reduce intracranial pressure in neurological conditions
  • reduce intraocular pressure before opthalmologic procedure
  • to counteract low osmolality of plasma /ECF due to rapid haemodialysis.
43
Q

Explain the loop of diuretics ( Furosemide) of mechanism of action

A
  • bind to luminal side of Na+/K+/ 2CL- cotransporter at thick ascending segment of loop of Henle and block its function ; it inhibits reabsoprtions of Na+ , Cl- —> Na+ and Cl- are retained in the lumen and excreted along the water .
  • increased Na+ concentration & now reaching the distal tubules promotes loss of H+ & K+
  • in high dose particularly may produce metabolise alkalosis
  • it also increase in the excretion of Ca2+ & Mg2+ due to inhibition of reabsorption of them.
44
Q

Lis the pharmacological action of loop diuretics

A
  • Increased Na+ excretion cause hyponatremia.
  • ( H2O) ….hypovolemia
  • (Ca2+) …..Hypocalcemia
  • ( K+ ) …..hypokalemia
  • (Mg2+) … hypomagnesemia
  • ( Cl-) ….. hypochloremia
  • *** - Decrease Uric acid excretion ……… hyperuricemia
45
Q

Explain the mechanism action of sodium chloride inhibitor ( Thiazide. )

A

A) binds to luminal side of Na+/ Cl- symport at the early distal tubules and block its function —> inhibit reabsorptions in the lumen and excreted along with water.

B) decrease the Ca2+ concentration of urinepromoting its reabsorption

C) Lowering of intracellular Na + ( due to its excretion by thiazides) enhances Na + - Ca 2+ exchange in absolute real membrane which in turn promotes overall reabsorption.

D)low ceiling diuretics

46
Q

List the therapeutics uses of thiazides

A

A) hypotension
B) pulmonary oedema due to congestive heart failure
C) Nephrolothiasis ( kidney stone)due to idiopathic hypercalciuria
D) Nephrogenic diabetes indipidus

47
Q

Explain the mechanism of action of digoxin

A

A)Na+ K+ ATPase is a pump which pumps out 3 Na+ ions out of cell and 2 K+ ions into the cell.
B) This helps in maintaining Na + out of the cell and maintain negative potential inside the cell
C) Digitalis compound blocks the Na+K+ ATPase pump
D) Which cause the increase in intracellular sodium level
E) Another pump called sodium calcium exchanger pumps out this extra Na+ out in exchange for Ca+ which moves inside.
F) So the intracellular calcium levels increase which cause contraction of the cardiac muscle leading to cardiac output.

48
Q

State the uses of digitalis

A
  • useful in systolic ( dilated ) and low output failure with decompensation ( when not controlled by diuretics )
  • control ventricular rate in atrial flutter and atrial fibrillation.
49
Q

List the adverse effect of digitalis

A

Cardiac : Cardiac arrhythmias , AV nodal blocks , sinus Bradycardia
GIT : nausea & vomiting
Eye : visual complaints ( coloured halos)
CNS : fatigue , headache
Endocrinologist : gynecomastia

50
Q

List oral & parental iron preparation to iron

A

Oral iron preparation

  • Ferrous sulphate , Ferrous fumarates ( 200mg tab)
  • Ferrous gluconate ( 300mg tab)
  • Ferrous succinate ( 100mg )
  • Iron calcium complex - 5% iron
  • Ferric ammonium citrate - 45mg

Parental iron preparation

  • Iron sorbitol citric acid complex given ***(IM but never IV )
  • Iron dextran complex + IV or IM ( Z- track techniques )
  • Ferric carboxymaltose and ferrous sucrose are administered IV
51
Q

List the therapeutic uses of iron preparation

A
  • to treat the iron deficiency anaemia. In anemia , the RBC are microcytic and hypochromic due to Hb synthesis ( microcytic hypochromic anaemia)
  • cause for iron deficiency should be identified before giving the treatment
    A) During pregnancy
    B) Due to Acute or chronic blood loss.
    C) Due to nutritional iron deficiency.
    D) Due to poor absorption of iron from the gut.

-iron should be normally administered orally ; parental therapy is to be reserved for special circumstances.

52
Q

List the prophylactic uses of iron preparations.

A 
Iron is required to meet increased demand in 
A) Professional blood donors 
B) Menstruating women 
C) Infants 
D) Chronic illness
53
Q

Explain the indication for parental therapy for iron

A

A) intolerance & non compliance to oral iron
B) Malabsorption of iron . Chronic inflammation ( rheumatoid arthritis) decrease iron absorption.
C) Severe iron deficiency . Anaemia in the late stages of pregnancy.
D) Patients with renal disease along with the erythropoietin therapy
D)

54
Q

List the adverse effect of iron preparation.

A

A) Oral preparation

  • Nausea
  • Vomiting
  • Epigastric pain
  • staining of teeth in liquid formulation
  • Constipation
B) Parental iron preparation 
I) Local 
- pain at injection 
- abscess 
- discolouration of the skin at site of injections

II) Systemic side effects

  • Lymphadenopathy
  • Anaphylactic reaction
  • Nausea and vomiting
55
Q

List various preparation of Vit B12

A

Parentally - Cyanocobalamin
- Hydroxocobalamin
Orally - Methylcobalamin

**never administered IV because of risk of anaphylaxis

56
Q

List the various preparation of folic acid

A
  • Folic acid and folinic acid
  • ** Folinic acid & calcium leucovorin) used in treatment of methotrexate toxicity and as adjuvant in methanol poisoning
57
Q

Mention the therapeutic uses of Vit B12

A

1) Pernicious anaemia ( Oral vitamin B12 is not absorbed because of the deficiency of IF )
2) Along with folic acid for Megaloblastic anaemia
3) Prophylactic therapy with Vit B12 is indicated in patients at high risk of developing deficiency ( patients who undergone gastrectomy)

58
Q

List the primary line and second line antitubercular drugs

A

First line drugs

  • Isoniazid (H)
  • Rifampicin ( R)
  • Pyrazinamide (Z)
  • Ethambutol (E)
  • Streptomycin

Second line drugs

  • Ciprofloxacin
  • Clarithromycin
  • Amikacin
  • Cycloserine
59
Q

List the adverse effect of Isoniazid ( INH) **

A

A) Peripheral neuritis
Slow acetylators —> decrease rate of acetylation of isoniazid —> less metabolism of isoniazid —> increased plasma level of isoniazid —> more prone to peripheral neuritis

1) decrease the pyridoxine kinase causes decrease of pyridoxal phosphate ( active form of pyridoxine )
2) increase excretion of pyridoxine in urine.

—> increase symptoms of peripheral neuritis like numbness & vitamin B6 deficiency

B) Hepatotoxicity
Fast acetylators (increased rate of acetylation of isoniazid —> more metabolism of isoniazid —> decreased plasma level of isoniazid —> more formation of hepatotoxic metabolites of isoniazid —> prone to hepatotoxicity )
- Reversible

Others adverse effects are anorexia , nausea, vomiting , fatigue , lethargy

60
Q

State the adverse effect of pyrazinamide

A

Hepatotoxicity , Hyperuricemia ( decrease renal excretion of urates and may precipitate gouty arthritis ) , abdominal distress

61
Q

State the adverse effects of ethambutol

A

A) Optic neuritis - retrobulbar neuritis impairing visual acuity and red - green colour discrimination

B) Hyperuricemia : Ethambutol decrease renal excretion of urates ad may precipitate gouty arthritis
C) abdominal distress , nausea , comiting

62
Q

State objective of multidrug therapy in TB

A

A) Kill dividing bacilli

  • make patient non contagious to the community
  • to afford quick symptoms relief

B) To kill persisting bacilli
-to effects cure and prevent relapse

C) To prevent the emergence of drug-resistant bacilli
D)To reduce the total duration of effective therapy

63
Q

Explain about the short course chemotherapy tuberculosis

A

It has 2 phase
A) Intensive phase - Aimed rapidly kill the bacteria , to minimise the cancer of developing resistance and to bring about sputum conversion and symptomatic relief. ( 4-5 antitubercular drugs daily or thrive weekly for a period of 2-3 months )

B) Continuation phase

  • aimed to eliminate the remaining bacilli and prevent relapse
  • Usually , 2-3 drugs daily or thrice weekly for a period of 4-5 months
64
Q

List the coagulants ( Local agents and systemic agents )

A

Local agents (Styptics)

  • Astringents
  • Adrenaline
  • Thrombin
  • Fibrin
  • Gelatin
  • Calcium Alginate
  • Oxidised cellulose
  • Russel’ s viper venom ( haemocoagulase )

Systemic agents
- Vitamin K

65
Q

Explain the mechanism of local haemostatics ( Styptics )

Astringent and adrenaline

A
  • Control bleeding from capillaries and minute vessels

A) Astringents :Precipitate proteins locally in the bleeding site and control capillary oozing ( Example : Tannic acid , ferric chloride , ferric sulfate , aluminium chloride , aluminium sulfate )

B) Adrenaline : Vasoconstriction and arrest bleeding .
-A cotton pad soaked in 0.1% adrenaline solution is applied on the bleeding sites to control capillary oozing ( Epitaxis , bleeding after tooth extraction or from other sides

  • Adrenaline should be avoided in patients with hypertension, congestive cardiac failure, arrhythmias , ischaemic heart disease and uncontrolled hyperthyroidism as it may precipitate myocardial infarction or aggravate
    the existing condition.
66
Q

State the therapeutic uses of local haemostatics

A
  • To stop superficial bleeding in patients with haemophilia
  • To stop bleeding from tooth socket
  • Epistaxis
  • Bleeding gums
  • Bleeding piles
67
Q

State the MOA of thrombin ( local haemostatics)

A

Thrombin : Freeze dried powder derived from bovine / human plasma . Applied topically during surgical procedure

68
Q

Explain the MOA of Fibrin and haemocogulase ( local haemostatics)

A

Fibrin : Consist of fibrinogen , factor XIII , thrombin , C2+ and other clotting component’s. it used to control bleeding during surgical procedure or as spray on bleeding surface. Fibrin sealant in combination with tranexamic acid mouthwash helps to reduce bleeding during dental extraction in haemophilic patients.

Haemocoagulase : haemocoagulase enzyme complex is isolated from the venom of Bothrops atrox ( viper )

69
Q

Explain the MOA of collagen and oxidised cellulose ( local haemostatics)

A

Collagen : It controls bleeding by promoting aggregation of platelets and accelerating coagulation . Collagen sponges are places in the tooth socket following extraction to arrest bleeding.

Oxidised cellulose : It is an absorbable haemostatics. it should be applied dry so that it swells up and helps in formation of clot. it used to control bleeding from capillaries and arteriolar where ligation is not possible. it may cause tissue necrosis , nerve damage or vascular stenosis.

70
Q

Explain the preparation of Vitamin K

A

1) Vit K - fat soluble vitamin found in liver , leafy vegetables and pulses

2) Essential in the biosynthesis of clotting factors.
- Factor II ( prothrombin )
- VII (proconvertin)
- IX ( Christmas factor )
- X ( Stuart factor)

Vitamin K -
A) K1 -Phytonadione
B) K2 - Menaquinone
C) K3 Menadione

71
Q

Explain the therapeutic uses of Vitamin K

A
  • Prolonged antimicrobial therapy
  • overdose of oral anticoagulant ( VIT K , 1mg , im )
  • Newborn of premature infants ( Vit K , 1mg ,im )
  • Obstruct jaundice or malabsorption syndromes
  • Liver disease
  • Hypoprothrombinemia cause by prolonged high dose salicylate therapy
72
Q

List the adverse effect of vitamin K

A
  • Oral vitamin K is safe
  • IV injection - flushing , sweating , dyspnoea , cynasosis ,collapse and anaphylactic reactions.
  • Menadione may cause Hemolysis , hyperbilirubinaemia and kernicterus in newborn
73
Q

Classify the anticoagulants based on their route of administration

A

A) Parental anticoagulants

  • High molecular weight heparin , unfractionated heparin / heparin
  • Low molecular weight heparins ( Enoxaparin , Dalteparin )
  • Thrombin inhibitor
  • Synthetic heparin derivatives

B) Oral,anticoagulants

  • Warfarin
  • Dicumarol
  • Direct oral anticoagulants/ Novel anticoagulants
74
Q

Explain the mechanism of action of heparin

A

1) HMWH binds with antithrombin III
2) Formation of HMWH-AT-III complex
3) HMWH induces a conformation change in AT-III to expose and make its reactive site more accessible for factor IIa/ Xa binding
4) HMWH-AT-III clotting factor ternary complex is formed
5) Blockade of activity of activated clotting factors
6) No blood clotting

75
Q

Explain about Heparin pharmacokinetics

A
  • Large , highly ionised molecule ; so that not absorbed from GIT . so it is given IV / SC
  • Does not cross blood brain barrier or placenta
  • Metabolized in liver and excreted through urine
  • Utilized for rapid and short lived action because of its short half life. ( For Acute situation)
76
Q

Explain about the low molecular weight heparin

A

Same with the HMWH

** But It induces conformation changes in AT-III to expose and make its reactive site more accessible for factor Xa binding only!!!

77
Q

Explain the therapeutic uses of heparin

A
  • Rheumatic heart disease
  • Unstable angina
  • Acute myocardial infarction
  • Prophylaxis and treatment for pulmonary embolism
78
Q

List the adverse effect of heparin

A
  • ** Heparin induced thrombocytopenia (HIT)
  • Haematuria ( first sign)
  • Bleeding - due to overdose of heparin therapy
  • Osteoporosis
79
Q

State the treatment of heparin overdose

A
  • discontinuation of heparin
  • Blood transfusion
  • Protamine sulphate *** is a specific antagonist for heparin overdose ( neutralise strongly heparin weight by weight ) (1 mg protamine = 100U of heparin
80
Q

State the advantages of LMWH vs heparin

A
  • Longer half life ( making possible once daily administration)
  • Do not prolong aPTT ( activated partial thromboplastin time )j and whole blood clotting time - Laboratory monitoring is not required as a routine
  • low risk of osteoporosis and Thrombocytopenia
  • Better subcutaneous bioavailability compared to HMWH
81
Q

Explain the MOA of warfarin

A

1) Competitively inhibit vitamin K oxide reductase ( VKOR)
2) Interferes with regeneration of the active hydroquinone form of vitamin K which acts as a cofactor for the enzyme gamma- glutamyl carboxylate that carries out the final step of gamma carboxylating glutamate residue of clotting factor II , VII , IX and X

3) No gamma carboxylation of clotting factor II , VII , IX ,X
4) No activation of clotting factors II, VII , IX and X
5) No blood clot formations ( Anticoagulant effect )

82
Q

Explain the pharmacokinetics of warfarin

A
  • well absorbed in orally
  • Crosses the placental barrier ( which affect the baby )
  • Long plasma half life
  • Metabolized in liver , undergoes enterohepatic circulation and partly conjugated with glucocorticoid acid and excreted in urine .
83
Q

Explain the warfarin drug interaction

A

ODEVICES ( drug that inhibit the metabolism of the warfarin and causes the increase warfarin concentration in the serum.
Omeprazole , Disulfiram , Erythromycin , Valproate , Isoniazid , Ciprofloxaxin , Ethanol , Sulphonamides

CP BARS ( Drugs that increase the metabolism of warfarin and causes decrease of warfarin in the serum ) 
Carbamazepine , Phenytoin , Barbiturates , Alcohol , Rifampicin , Sulphonylureas
84
Q

State the treatment of warfarin overdose

A
  • Withhold warfarin
  • Give fresh blood transfusion ( Supplies clotting factors and replenishes lost blood. Fresh frozen plasma or factor IX concentrate maybe used as a source of clotting factors.

-Give vitamin K1 (phytonadione ) *** which is specific antidote . It takes 6-24 hours for the clotting factors to,be synthesised and released in blood after Vitamin K administration.

85
Q

List the antiplatelet drugs based on their MOA

A

A) Thromboxane A2 inhibitor - Aspirin
B) Phosphodiesterase inhibitor - Cilostazol
C) ADP receptor antagonists - Clopidogrel
D) GPIIb / IIIa antagonists : Abciximab , Eptifibatide

86
Q

Explain the MOA of Aspirin ( Thromboxane A2 inhibitor )

A
  • Inhibit COX enzyme and thereby the synthesis of prostaglandins from arachidonic acid.
  • Most important prostaglandins affecting platelet aggregation are prostacyclin and Thromboxane A2 ( TXA A2)
    : Prostacyclin is produced by intact endothelial cell and inhibits platelet aggregation.
    : TXA2 is produced by platelets and promoted platelet aggregation
  • Low doses of aspirin ( 75- 150mg) selectively inhibit TXA2 synthesis from platelets and reduces platelet aggregation.
  • Aspirin irreversibly inhibits COX (unlike other NSAIDsj and since platelets cannot synthesis new COX enzyme , platelets are inhibited for their life
  • Aspirin
87
Q

State the uses of aspirin

A
  • Prevent Arterial thrombosis in patients with IHD , stroke
  • In patients with previous Mi or stroke
  • In patients with transient ischemic attack (TIA )
  • In patients with artificial heart valves
  • Patients undergoing percutaneous coronary angioplasty
88
Q

Adverse effect of aspirin

A
  • Bleeding especially in GIT

- Gastric and peptic ulcers

89
Q

Explain the MOA of ADP inhibitors

A
  • Clopidogrel blocks platelet adenosine diphosphate P2Y12 receptors
  • Prevent ADP-induced platelet aggregation
90
Q

Explain the MOA of GPIIb/ IIIa inhibitor

A
  • The final common pathway in platelet aggregation is cross-linking of platelets by fibrinogen to activated GPIIb/IIIa receptors
  • Abciximab , eptifibatide

Vorapaxar (new drug)

  • Protease activated receptor 1 antagonist (PAR-1 antagonist)
  • By occupying the PAR-1 receptor , vorapaxar competitively inhibit thrombin access to its target receptor and prevents thrombin - mediated platelet aggregation
91
Q

Classify potassium sparing diuretics

A

Aldosterone antagonists :

  • Spironolactone
  • Eplerenone

Direct inhibitor of sodium channels :

  • Amiloride
  • Triamterene
92
Q

List the aldosterone antagonist ( potassium sparing diuretics )

A
  • Spirolactone competes for aldosterone receptors in the cells of late distal tubules and collecting duct and binds to it.
  • Transcription , translation & production of aldosterone induced protein (AIPs include Na+-K+ ATPase and renal epithelial Na+ channels) are inhibited.
  • Inhibit activation of Na+ channels and their translocation from cytotoxic site to luminal membrane and inhibitions of Na+-K+ ATPase to the basolateral membrane.
  • Results in inhibition of Na+ reabsorption and concomitant decrease in K+ secretion.
93
Q

Explain the mechanism of action of Amiloride ( direct inhibitor of sodium channels )

A

1) Amiloride inhibit luminal Na + channels at late distal tubules and collecting duct.
2) Inhibit Na+ reabsorption
3) Decreases lumen negative potential which is the driving force for K+
4) K+ excretion is prevented indirectly to a significant level

94
Q

List the adverse effect of Rifampicin

A
  • Hepatitis , Flu like syndrome , Abdominal syndrome , Cutaneous syndrome , Urine and body secretions may become orange-red
95
Q

Explain how drugs lower blood pressure

A

BP = Cardiac output x peripheral resistance

1) Dilating arteriolar resistance vessels
- Vasodilator , increase NO , blocking endogenous vasoconstrictors

2) Dilating venous capacitance vessels , reduces preload and reduces cardiac output
3) Reduction of cardiac contractility and heart rate
4) Reducing the volume of blood

Pharmacology (4 decks)

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